HUGO ID Detailed Result 6881

PMID	Match String	Actual String	Score	Flanking text	Edited by	Edit
16227974	JNK	JNKs	0.3	cytosolic stress pathways (for for example Jun N-terminal kinases (JNKs) JNKs and p38
17496232	JNK	JNK	2.7	MAPKs including SAPK/JNK, SAPK JNK p38 MAPK and ERK are believed to be redox-dependent biomolecules
17496232	JNK	JNK	2.7	that H 2 O 2 -induced cellular injury depends on JNK activation
17496232	JNK	JNK-related	2.7	ERK were activated by H 2 O 2 however only JNK-related injuring effects were inhibited by the MEK inhibitor PD-98059
17496232	JNK	JNK	2.7	Moreover JNK phosphorylation of p53 is important for the stabilization of proapoptotic
17496232	JNK	JNK	2.7	and that Ca -dependent tyrosine kinase-induced activation of SAPK/JNK SAPK JNK reflects the progression of cell injury ( 73
17496232	JNK	JNK	2.7	NO induces apoptotic cell death with the activation of JNK/SAPK JNK SAPK and p38 MAPK and caspase 3 or inactivation of
17496232	JNK1	JNK1	2.7	Because proapoptotic p38 or JNK1/2 JNK1 2 did not become phosphorylated we surmise the results are
17634371	JNK	JNK	0.6	but is associated with activation of c-Jun N-terminal kinase (JNK), JNK release of cytochrome c from mitochondria and subsequent activation of
17634371	JNK	JNK	0.6	hippocampal neurons involving nSMase activation increased ceramide generation and subsequent JNK activation (Brann Brann et al. 2002